ESR2 and inflammatory breast carcinoma: Since ERβ has already been shown to transcriptionally downregulate another G protein-coupled receptor—GPR141—to inhibit actin-based migration in inflammatory breast cancer [65], there is a possibility of functional crosstalk between ERβ and GPER or other GPCRs, where ERβ might oppose EGFR signaling by inhibiting the expression and activity of GPER.